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Time FIGURE 2. A comparison of percent predicted FVC in six subjects over a four-year period following cadmium chemical pneumonitis. Patients A,· B,· C,· 0,8 E (present report), RIO

Frequently, the worker is unaware that the metal being cut, burned, or brazed contains cadmium. Physical, laboratory and radiographic abnormalities consistent with non-eardiogenic pulmonary edema all support the diagnosis of chemical pneumonitis. The treatment is supportive and although its clinical efficacy is not established some authors have advocated the use of corticosteroids. 13 Determining the cause of the pneumonitis may be more difficult. In this case, the setting strongly suggests cadmium, but phosgene (from chlorinated hydrocarbons and heat) or other gases also need to be considered. Analysisof the fumes or the material being used is best. Biological determinations are difficult to interpret and are much less satisfactory. Blood levels correlate best with acute exposures and urine levels are probably a better reflection of the total body burden. Blood or urine cadmium levels which are above. 005 mg/L suggest excessive exposure. 14 Chemical pneumonitis secondary to the inhalation of cadmium fumes is a potentially lethal syndrome and is associated with long-term adverse respiratory sequelae. Given the markedly different clinical course but nearly identical presentation, cadmium pneumonitis needs to be considered in any patient presenting with the signs and symptoms of metal fume fever. Aswith most diseases of the workplace, the best treatment is prevention and should include, in addition to technological improvements in the workplace, worker education about

potential hazards of welding, appropriate ventilation, and if necessary use of personal protective equipment. REFERENCES

1 Parkes WR. Non-neoplastic disorders due to metallic, chemical and physical agents. In: Parkes, WR, Occupational lung disorders, 2nd ed. London: Butterworths, 1982:457-63 2 Beton DC, Andrews GS, Davies HJ, Howells L, Smith GE Acute cadmium fume poisoning. Br J Ind Med 1966; 23:292-301 3 Johnson JS, Kilburn KH. Cadmium induced metal fume fever: results of inhalation challenge. Am J Industr Med 1983; 4:533-40

4 LeeJS, White KL. A review of the health effects of cadmium. Am J Industr Med 1980; 1:307-17 5 Smith TJ, PettyTL, Reading Je, Lakshminarayan S. Pulmonary effects of airborn cadmium. Am Rev Respir Dis 1976; 114:161-69 6 Patterson JC. Studies on the toxicity of inhaled cadmium. J Industr Hyg Tox 1947; 29:294-301 7 lavon MR, Meadows CD. Vascular sequelae to cadmium fume exposure. Am Ind Hyg Assoc J 1970; 31:180-82 8 Anthony JS, Zamel N, Aberman A. Abnormalities in pulmonary function after brief exposure to toxic metal fumes. Can Med Assoc J 1978; 119:586-88 9 Blejer J~ Caplan PE, Alcocer AB. Acute cadmium fume poisoning in welders-a fatal and a nonfatal case in California. Calif Med 1966; 105:290-96 10 Townshend RH. A case of acute cadmium pneumonitis: lung function tests during a four-year follow-up. Br J Ind Med 1968; 25:68-71 11 Strauss RH, Palmer KC, Hayes JA. Acute lung injury induced by cadmium aerosol. Am J Patho11976; 84:561-78 12 Palmer KC, Snider GL, Hayes JA. Cellular proliferation induced in the lung by cadmium aerosol. Am Rev Respir Dis. 1975; 112:173-79 13 Dunphy B. Acute occupational cadmium poisoning. J Occ Med 1967; 9:22-6 14 Baselt RC. Biological monitoring methods for industrial chemicals. Davis: Biomedical Publications, 1980:53

Systolic Anterior Motion of the Mitral Valve* An Unusual Echocardlographlc Feature

of Mitral Valve Endocarditis

Francesco Enia, M.D.; Renato Lo Mauro, M.D.; and Enrico Geraci, M.D.

An unusual M-mode ecbocardiographic feature of mitral valve endocarditis is described: systolic anterior motion of the mitral valve, likely due to mitral valve vegetations, protruding during systole into the left ventricular outflow tract. The presence of mitral valve vegetation was con6rmed at operation. anterior motion of the mitral valve (SAM) was the Systolic first echocardiographic abnormality observed in hyper-

trophic cardiomyopathy" This finding was considered to represent echocardiographic evidence of the left ventricular outflow tract obstruction seen in hypertrophic cardiomyopathy and was promoted for the measurement of this obstruction." Subsequently, there were increasing reports of patients who showed SAM without evidence of hypertrophic cardtomyopathy.P" We describe a patient with SAM as an

echocardiographic feature of mitral valvevegetations. Wedid not find similar reports in the literature, except an unpublished observation by Rakowskiand Gilbert, quoted by Gilbert et al." CASE REPORT

The patient was a 48-year-old man with mitral regurgitation, *From the Division of Cardiology, Ospedale ~ Cervello, Palermo, Italy. Reprint requests: Dr: Enia, via F. Uszt 47, 90145 Palermo, Italy CHEST I 86 I 5 I NOVEMBER. 1984

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l ' l l ll-U II I J'l fit l 1.1' FIGURE 1. M-mode echocardiogram, performed ten days after hospitalization, showing aortic (A)and mitral valve (B) vegetations, with coarse systolic anterior motion of the mitral valve vegetation echo. which was cons idered "rheumatic." The echocardiographic examination before hospitalization showed neither mitral prolapse nor SAM. The patient was well until two months before hospitalization, when there was abrupt onset of low grade fever, weakness, arthralgias, weight loss and dyspnea. On examination, peripheral edema, pulmonary rales and moderate hepatomegaly were present. Cardiac auscultation revealed a grade 216 pan systolic murmur at the apex. Blood cultures grew Streptococcus oiridans. M-mode echoeardiography showed mitral valve vegetations (Fig IB), with coarse SAM of the mitral valve (Fig 3). The mitral valve vegetation echo moved in systole nearly up to the interventricular septum and returned to the baseline before the onset of ventricular diastole. There was no echocardiographic evidence of hypertrophic cardiomyopathy. Ten days after, while the patient was rece iving appropriate antibiotic therapy, aortic regurgitation , which was absent on admission, was detected. The aortic regurgitation murmur was incon stant at the onset, but later became stable. We could also detect probable aortic valve vegetations on M-mode echo (Fig lA), which were absent

FIGURE 2. Surgically removed anterior mitral leaflet exhibiting healed vegetations on the ventricular surface.

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on admission. Two-dimensional echocardiography confirmed the presence of mitral and aortic valve vegetations. The patient's condition improved with therapy. Angiography, performed three months later, showed moderate mitral regurgitation and severe aortic regurgitation. There was no intraventricular pressure gradient. The echocardiographic pattern was unchanged. At operation, the aortic valve showed small healed vegetations and an aneurysm of the right coronary cusp with two perforations. The mitral valve showed healed vegetations on the ventricular surface of the anterior leaflet (Fig 2). There was neither perforation nor ruptured chordae tendineae. Replacement of aortic and mitral valves was performed with Bjork-Shiley prostheses. The postoperative course was uncomplicated. DISCUSSION

Systolic anterior motion is now well recognized to be a nonspecific finding. P" It has previously been described in patients with aortic regurgitation and mitral valve prolapse.... Either or both of these conditions could be responsible for our observation. However, the followingpoints argue against these two causes of SAM in our patient: 1) the echocardiographic pattern of SAM resembled the typical coarse pattern of vegetations; 2) the echocardiographic examination before infective endocarditis showed neither mitral prolapse nor SAM; 3) the SAM was evident during infective endocarditis before the onset of aortic regurgitation . The latter was likely caused by the mycotic aneurysm of the right aortic cusp and its subsequent perforation. We believe that the SAM reported here was likely due to mitral valve vegetations protruding during systole into the Systolic Anterior Motion of Mitral valve (Enia, La Mauro , Geraci)

Obstructive Sleep Apnea and Abnormal cephalometric

Measurements*

Implications for Treatment Christian Guilleminault M.D.; Robert Riley, M.D.; and Nelson PoweU, M.D.

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The position of the hyoid bone, which anchors much of the tongue musculature, is often abnormally low in patients with obstructive sleep apnea syndrome (OSAS~ Cephalometric measurements, frequently used to measure SNA and SNB angles, can also provide information on the posterior airway space (PAS), the mandibular plane, and the hyoid bone. This information is useful in determining the appropriate surgical treatment for OSAS patients. sleep apnea syndrome (OSAS) is a comT heplexobstructive problem that may involve oronasomaxillofacial ab-

normalities. 1 We recently reported on the usefulness of obtaining systematic cephalometric roentgenograms when evaluating patients with OSAS.2 Evaluating the position of the mandibular plane (MP) with respect to the hyoid bone (H) may be of importance when dealing with OSAS. Before considering surgical treatment for OSAS, cephalometric measurements including not only the posterior airway space (PAS) but also the distance between the MP and the H should be obtained. MATERIAL AND METHODS

FIGURE 3. M-mode echocardiogram showing constant presence of SAM on three continuous strips.

left ventricular outflow tract. Hence, mitral valve vegetations can be considered another cause of true SAM. REFERENCES

1 Shah PM, Gramiak R, Kramer DU. Ultrasound localization of left

ventricular outflow obstruction in hypertrophic obstructive cardiomyopathy. Circulation 1969; 40:3-11 2 Henry WL, Clark CE, Giancy DL, Epstein SE. Echocardiographic measurement of the left ventricular outflow gradient in idiopathic hypertrophic subaortic stenosis. N Eng} J Med 1973; 288:989-93

3 Mintz GS, Kotler MN, Segal BL, Parry WR. Systolic anterior motion of the mitral valve in the absence of asymmetric septal hypertrophy. Circulation 1978; 57:256-62 4 Maron BJ,Gottdiener JS, Perry LW. Specificity of systolic anterior motion of anterior mitral leaflet for hypertrophic cardiomyopathy. Br Heart J 1981; 45:206-12 5 Gardin JM, Talano J~ Stephanides L, Fizzano J, Lesch M. Systolic anterior motion in the absence of asymmetric septal hypertrophy. A buckling phenomenon of the chordae tendineae. Circulation 1981; 63:181-88 6 Gilbert BW, Pollick C, Adelman AG, Wingle ED. Hypertrophic cardiomyopathy: subclassification by M-mode echocardiography. Am J Cardioll980; 45:861-72

Thirty randomly selected adult patients with documented OSAS were studied over a six-week period. All had an apnea-hypopnea index (A+ HI) (defined as the number of apnea and hypopnea divided by total sleep time and multiplied by 6
Cephalometric Roentgenograms Cephalograms were obtained while the patient, who was asked not to chew or swallow, was in a sitting position. The patient's eye looked directly forward from a natural head position so that the gaze was parallel to the 800r with the x-ray cone exactly five feet from the 81m placed on the left side of the head." Cephalograms provided millimetric determination of craniomaxillofacial struetures'" (Fig 1). We have used this technique to determine the length of a patients uvula and PAS.2 By drawing a line perpendicular to the MP (Fig 1) through the most anterior and superior curvature of the H, one can also establish the position oftheH vis-a-vis the ME ·From the Stanford University Sleep Disorders Clinic, Head-Neck Surgery, Palo Alto, CA. CHEST / 88 / 5 / NOVEMBER. 1984

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